Bertram E H, Zhang D X, Mangan P, Fountain N, Rempe D
Department of Neurology, Health Sciences Center, University of Virginia, Charlottesville 22908, USA.
Epilepsy Res. 1998 Sep;32(1-2):194-205. doi: 10.1016/s0920-1211(98)00051-5.
The limbic/mesial temporal lobe epilepsy syndrome has been defined as a focal epilepsy, with the implication that there is a well defined focus of onset, traditionally centered around the hippocampus. The pathology of the hippocampus in this syndrome has been well described and a number of physiological abnormalities have been defined in this structure in animal models and humans with epilepsy. However, anatomical and physiological abnormalities have also been described in other limbic sites in this form of epilepsy. Previous studies have shown broadly synchronized or multifocal seizure onset within the limbic system of the animal models and human patients. We hypothesized that the epileptogenic circuit for the initiation of seizures was distributed throughout the limbic system with a possible central synchronizing process. In vitro studies showed that multiple limbic sites in epileptic animals (hippocampus, entorhinal cortex, piriform cortex and amygdala) have epileptiform changes with prolonged depolarizations and multiple superimposed action potentials. In vivo studies revealed that thalamic stimulation yields short latency excitatory responses in the entorhinal cortex and hippocampus. In addition, in epileptic animals, thalamic stimulation caused epileptiform responses in the hippocampus. Based on the findings of this study and on previous anatomy and physiology reports, we hypothesize that the process of seizure initiation involves broad circuit interactions involving multiple independent limbic structures, and that the midline thalamus may act as a physiological synchronizer. We offer a new proposal for the functional anatomy of limbic epilepsy that takes widespread hyperexcitability in the limbic system and the potential for thalamic synchronization into consideration.
边缘系统/内侧颞叶癫痫综合征被定义为局灶性癫痫，这意味着存在一个明确的起始灶，传统上以海马体为中心。该综合征中海马体的病理学已得到充分描述，并且在癫痫动物模型和人类的该结构中已确定了一些生理异常。然而，在这种癫痫形式的其他边缘部位也描述了解剖学和生理学异常。先前的研究表明，动物模型和人类患者的边缘系统内存在广泛同步或多灶性癫痫发作起始。我们假设癫痫发作起始的致痫回路分布在整个边缘系统中，并存在一个可能的中央同步过程。体外研究表明，癫痫动物的多个边缘部位（海马体、内嗅皮质、梨状皮质和杏仁核）存在癫痫样改变，伴有延长的去极化和多个叠加的动作电位。体内研究显示，丘脑刺激在内嗅皮质和海马体中产生短潜伏期兴奋性反应。此外，在癫痫动物中，丘脑刺激在海马体中引起癫痫样反应。基于本研究的结果以及先前的解剖学和生理学报告，我们假设癫痫发作起始过程涉及多个独立边缘结构的广泛回路相互作用，并且中线丘脑可能起到生理同步器的作用。我们提出了一种关于边缘性癫痫功能解剖学的新观点，该观点考虑了边缘系统中广泛的过度兴奋性以及丘脑同步的可能性。
